pneumonia

pneumoniajourn

Vol7SpecialIssueforweb

EuroPneumo Special Issue / pneumonia 2015 Oct 21;7:I–72

overt pneumococcal disease. Increasing data demonstrate

an important role of the respiratory microbiome in

shaping local immune responses to S. pneumoniae at the

mucosal surfaces [8], and these effects are likely to have

wide-reaching consequences during carriage and disease

development. The importance of the interplay between

both bacterial and host factors in determining virulence

was nicely demonstrated through the reported use of

the less pathogenic S. mitis to assess host response in

comparison to S. pneumoniae [9]. Likewise, the potential

for the S. pneumoniae toxin pneumolysin to subvert the

early host inflammatory response [10,11] and cause direct

cardiac damage [12] confirms that bacterial-mediated

disruption of host cells can also be a key determinant in

the pathogenesis of infection.

After a conference with such varied content, what can

we conclude about future directions for research into S.

pneumoniae? Firstly, S. pneumoniae biology remains a

highly energetic and innovative field with an increasing rate

of novel and exciting discoveries. Secondly, and perhaps

paradoxically, the more we learn about S. pneumoniae

the more apparent it becomes how much more we

need to know. For example, genome sequencing has

identified much larger genetic variation between strains

than expected [13], and the effects of the microbiome

has added an additional layer of complexity to assessing

host immunological responses to S. pneumoniae [8].

Considerably more research will be required if we are

to state with confidence why S. pneumoniae is a highly

successful pathogen and before we learn how to prevent it

from causing such a huge level of morbidity and mortality

across the globe.

FFunding: AB is supported by funding from the Wellcome Trust

Biomedical Research Fund (Grant 04992/Z/14/Z), Wellcome Trust Career

Development Fellowship (Grant 83511/Z/07/Z), GlaxoSmithKline (GSK)

Biologicals (Grant HBRYVH00) and the University of Oxford John Fell

Fund (Grant 123/734). TM is supported by funding from the Wellcome

Trust Medical Research Council (Grant WT094762MA) and Department

of Health, UK (Grant MR/K012053/1). JB is supported by funding from

the Medical Research Council UK, Biotechnology and Biological Sciences

Research Council, National Health and Medical Research Council (Grant

1034029), Rosetrees Trust, Research Council of Norway, Meningitis Now

and the Department of Health’s National Institute for Health Research

(NIHR) Biomedical Research Centre. The funders had no role in study

design, collection and analysis of data, decision to publish, or writing of

the manuscript.

Competing interests: JB has received consultancy fees from

ImmunoBiology Ltd and Pfizer. AB has received grant support from GSK.

All other authors declare no competing interests.

JB, AB, TM were organisers of the EuroPneumo Conference.

Provenance and peer review: Commissioned; internally peer

reviewed.

Copyright: This is an open-access article distributed under the terms of

the Creative Commons Attribution License, which permits unrestricted

use, distribution, and reproduction in any medium, provided the original

author and source are credited.

References

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2015;7:58

pneumonia 2015 Volume 7

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